Scientists often revisit prior research work. Why do they do this? Probably because the ‘older’ work takes on new relevance as newer discoveries are made.

One such marker that was established many years ago, was identified by Ismael Mena, M.D. and colleagues at the UCLA Medical Center. The marker, cerebral hypoperfusion, had been previously identified in patients with CFIDS/ME. This work dates back to the early 1990’s and was completed with the assistance of the former Medical Director for the NCF, Jay Goldstein, M.D. [1].

In this study, 46 patients and 10 controls were selected for perfusion studies using neuroSPECT scans. SPECT is the acronym for Single Photon Emission Computed Tomography, an advanced nuclear imaging technique that is able to provide true 3D information. This technology utilizes a nuclear xenon tracer (133Xe) to quantify cerebral blood flow.

The neuroSPECT results had identified cerebral hypoperfusion in 71% of patients which was found to be statistically significant (p<0.001). Furthermore, this cerebral hypoperfusion was not sex related — no differences were found between male versus female patients regarding hypoperfusion.

Why is this intriguing? Probably because ischemia and tissue oxygenation are paramount to proper brain functioning where the importance of appropriate microcirculation cannot be understated. After all, the brain acts as the control center for all bodily functions. Unfortunately, if the brain takes a ‘hit’ then there can be numerous downstream effects as a result.

Interestingly, hypoperfusion is a known characteristic in AIDS dementia and HIV-related encephalopathy as well as Alzheimer’s disease [2 -5 ]. Thus, hypoperfusion may be a key prognostic indicator that characterizes pathological changes that occur in the brain in CFIDS/ME just as it does in AIDS and Alzheimer’s. Furthermore, CFIDS/ME brain fog, experienced by so many patients, may be related to and reflective of inadequate brain perfusion.